GMP BMP-2 Protein, Human/Mouse/Rat

Bone morphogenetic protein 2 (BMP-2) is a pleiotropic ligand protein belonging to TNFβ family, and is involved in key embryonic development of vascular and valvular homeostasis. BMP-2 binds to type I receptors (ALK-2/-3/-6) and type II receptors (BMPR2, ACVR2A) to regulate various types of calcification, including atherosclerosis, chronic kidney disease, diabetes, and valve calcification^[1]. BMP-2 is overexpressed by myofibroblast and preosteoblast in the calcified area of human calcified valve, which are densely infiltrated by B lymphocytes and T lymphocytes^[2]. BMP-2 is the junction between atherosclerotic vascular calcification and normal bone formation mechanism^[3]. BMP-2 Protein, Human/Mouse/Rat is 114 a.a. (Q283-R396), expressed in E. coli.

Bone Morphogenetic Protein 2 (BMP-2) is a ligand protein with pleiotropic, belongs to TNFβ family. BMP-2 formats BMP/TGFβ signaling to involve in vascular and valvular homeostasis, which is a critical process of embryonic development^[1].
BMP-2/TGFβ signaling can be terminated by inhibitory SMADs including SMAD6 and SMAD7, which are activated and induced by BMP signaling and switch off BMP signaling via multiple mechanisms^[4].
BMP-2 is widely found in different animals, while the sequence in human is similar to Rat (91.86%), and mouse (92.13%).
BMPs exhibits critical contributions to the pathophysiology of atherosclerosis, pulmonary vascular disease, and vascular and valvular calcification^[1].
BMP-2 binds different receptor, such as type I receptors (ALK-2/-3/-6) and type II receptors (BMPR2, ACVR2A), to regulate various calcification type including Atherosclerosis, Chronic Kidney Disease, Diabetes, Valvular Calcification^[1].
BMP-2 promotes monocyte infiltration and inflammation of atherosclerotic legions^[5].
It is linked to increased plaque formation via pro-inflammatory and pro-atherogenic effects, promoting oxidative stress, endothelial dysfunction and osteogenic differentiation^[6].
BMP-2 is overexpressed in ossified regions of human calcified valves by myofibroblasts and pre-osteoblasts in areas densely infiltrated with B- and T-lymphocytes^[2].
And it serves as the linkers between atherosclerotic vascular calcification with mechanisms of normal bone formation^[3].
BMP-2 induces angiogenesis, endothelial cells (ECs) proliferation, and migration^[7].
And BMP-2 also enhances the expression of the osteoblast and chondrocyte master transcriptional regulator RUNX2 to promote the mineralization of cultured human coronary vascular SMCs in a manner that was dependent on oxidative stress and endoplasmic reticulum (ER) stress^[8].

BMP-2 (10 nM; 15 min) shows little effect on the phosphorylation of MADR1, indicating MADR1 is a downstream component in the BMP2 signal transduction pathway^[9].
BMP-2 (50 ng/mL; 14 d) induces osteogenic differentiation of mesenchymal stem cells (MSCs) as well as strong synergistic effect with 1 ng/mL VEGF and 10 ng/mL bFGF, in bone marrow of femurs and tibias of 6 week-old rats^[10].

Human; Rat; Mouse

E. coli

Tag Free

P12643 (Q283-R396)

650

Full Length of Mature Protein

QAKHKQRKRLKSSCKRHPLYVDFSDVGWNDWIVAPPGYHAFYCHGECPFPLADHLNSTNHAIVQTLVNSVNSKIPKACCVPTELSAISMLYLDENEKVVLKNYQDMVVEGCGCR

Approximately 13 kDa, based on SDS-PAGE under reducing conditions.

Greater than 95% as determined by reducing SDS-PAGE.

<0.1 EU/μg, determined by LAL method.